In this study we demonstrated that combining the MEK inhibitor pimasertib with the PARP inhibitors olaparib and rucaparib increased DNA damage and induced antiproliferative responses in BRCA2-wild type ovarian cancer cell lines, indicating that MEK inhibitors could be used as a therapeutic strategy to produce a ‘BRCAness’ phenotype [9] that would sensitize BRCA2 wild-type proficient tumors to PARP inhibition. The gene discussed is BRCA2; the disease is ovarian carcinoma.